| Literature DB >> 29847549 |
Noah Haber1,2, Emily R Smith1,3, Ellen Moscoe1,4, Kathryn Andrews1,2, Robin Audy5, Winnie Bell6, Alana T Brennan7,8, Alexander Breskin9, Jeremy C Kane10, Mahesh Karra1,11, Elizabeth S McClure9, Elizabeth A Suarez9.
Abstract
BACKGROUND: The pathway from evidence generation to consumption contains many steps which can lead to overstatement or misinformation. The proliferation of internet-based health news may encourage selection of media and academic research articles that overstate strength of causal inference. We investigated the state of causal inference in health research as it appears at the end of the pathway, at the point of social media consumption.Entities:
Mesh:
Year: 2018 PMID: 29847549 PMCID: PMC5976147 DOI: 10.1371/journal.pone.0196346
Source DB: PubMed Journal: PLoS One ISSN: 1932-6203 Impact factor: 3.240
Inclusion criteria.
| Media article: | Academic article: |
|---|---|
| • The URL link to media article is functional at the time of the review, leading to the main media article. | • The academic article referred to in the media article is identifiable through academic library sources. |
Fig 1Results of summary measures for strength of causal inference and language.
Language for categories of strength of causal inference has been lightly edited for this publication to better reflect the instructions given to the reviewers and for consistency with the rest of the manuscript. Reviewers were instructed to consider only the causal inference aspect of the study for these measures. The original language referred to the “study” and “results,” which has been edited in the figure to “causal inference” where appropriate for clarity. The original language and instructions are available in the attached review tool and on metacausal.com.
Academic article descriptive statistics.
| % (n) | % (n) | |||
| Randomized controlled trial | 14% (7) | Standard correlation | 80% (40) | |
| Standard RCT | 86% (6) | Hierarchical/longitudinal | 20% (10) | |
| Crossover trial | 14 (1) | Instrumental variable | 2% (1) | |
| Observational | 82% (41) | Marginal structural model | 2% (1) | |
| Prospective cohort | 54% (22) | Can't be determined | 2% (1) | |
| Cross-sectional | 31% (13) | Other | 10% (5) | |
| Case-control | 5% (2) | |||
| Retrospective cohort | 2% (1) | n | ||
| Ecological | 2% (1) | 25th percentile | 326.5 | |
| Other | 5% (2) | Median | 5,143.5 | |
| Other | 4% (2) | 75th percentile | 34,849 | |
| % (n) | % (n) | |||
| Built environment | 10% (5) | Mood / Mental health | 20% (10) | |
| Diet | 10% (5) | CVD | 14% (7) | |
| Coffee / Caffeine | 8% (4) | Cognitive function / Schooling | 10% (5) | |
| Medical device / Treatment | 8% (4) | Mortality | 10% (5) | |
| Pregnancy / Delivery | 8% (4) | Self-rated Health | 8% (4) | |
| Pet / Animal-related | 6% (3) | Weight/BMI | 8% (4) | |
| Race / Ethnicity / Sex / Gender | 6% (3) | Blood biomarkers (multiple) | 4% (2) | |
| Air pollution | 4% (2) | Cancer | 4% (2) | |
| Marriage / Partnership / Children | 4% (2) | HIV | 4% (2) | |
| Mindfulness / Meditation / Yoga | 4% (2) | |||
| Other | 32% (16) | Other | 18% (9) | |
Data from panel a directly reflects the categorizations of study types and methods reviewers were given in the review tool, where the results shown are the arbitrator-determined categorizations. Additional details on the categories are available in the review tool itself, provided as a supplement, and in the Review Tool section of this manuscript. Panel b reflects categories determined post-hoc by the study authors, given the arbitrator-reported exposures and outcomes. The uncategorized reviewer-listed outcomes and exposures are provided in the publicly available datasets.
Fig 2Summary of severity of issues in causal estimate in academic article by category.
Fig 3Strength of causal inference vs. strength of causal language in academic and media articles.
The upper charts represent an assumed set of theoretically preferred regions, where we would prefer studies of the form exposure vs. outcome which reach the public to have language matching the strength of causal inference, a slight preference towards stronger causal inference, media language matching the academic language, and a preference for understated vs. overstated strength of causal language. The lower charts represent the empirical results of the study, where darker regions have more articles. The raw number of articles in each box is available in supplemental S4 Table.
Hypotheses supported and not assessed or supported by this study.
| Primary study conclusions drawn from the main objectives, design, and results of this study. Replication, validation, and critical review of the methods and conclusions by independent parties are still necessary before results should be considered conclusive. | - The academic articles assessing the relationship between an exposure and health outcome that were most shared on social media in 2015 have, on average: |
| This study DOES NOT assess these hypotheses. Reporting any of these conclusions as a result of this study is inaccurate and a misrepresenting the results and conclusions of this study. At most, these hypotheses remain plausible given the results of this study, and could be considered hypothesis-generating. However, additional review studies specifically designed to assess these questions are necessary in order to add any substantial weight to these hypotheses. | - Academic institutions, including researchers, universities, and journals, produce mostly weak and/or overstated evidence. |